Depigmenting agents, also called demelanizing agents, are well known, and currently include hydroquinones and catechols. See L. Goodman and A. Gilman, The Pharmacological Basis of Therapeutics, 954-55 (A. Gilman, L. Goodman, T. Rall and F. Murad, 7th ed. 1985) (hereinafter "Goodman and Gilman"); see also Bleehen, S.S., Depigmentation of skin with 4-isopropylcatechol, mercaptoamines and other compounds, J. Invest. Derm. 50, 103 (1968).
Contraindications and other undesirable effects of compounds such as hydroquinone, however, indicate a continuing need for alternative depigmenting agents. The ability to spontaneously induce depigmentation in an animal would, in addition, eliminate the need for genetically fixing this trait, if so desired, in a population of animals. The latter is very time consuming and cannot be done at all in species where albino individuals have not been observed. Some of the other applications of this technique include the production of lighter colored food fish (consumers prefer lightly colored fish over their darker counterparts), white pelts from fur-bearing animals, and the biological tagging of animals.
The cutaneous depigmentation caused by the topical application of the known depigmenting agents is caused by a selective cytotoxic action. See Goodman and Gilman, supra at 954. Melanin-pigmented cells are unique in that they possess tyrosinase, a polyphenol oxidase that converts tyrosine to melanin through a series of oxidation reactions. The great majority of known depigmenting agents have a highly reactive quinol moiety as a common structural feature. It is hypothesized that these agents exert their selective cytotoxic effects by a conversion of the quinol by tyrosinase to a quinone and ultimately to a semiquinone (Semiquinones are free radicals which are believed to react with certain enzymes essential to cells, such as DNA dependent DNA polymerase). Unfortunately, the usefulness of these compounds is limited by their toxic side effects.